Turning on the Insulin Switch in Type 2 Diabetes

People who eat a high-fat, high-sugar “Western” diet typically exhibit physiological changes associated with type 2 diabetes. However, not everyone responds the same way to the Western diet; genetics plays a strong role in determining one’s susceptibility to develop diabetes.

In type 2 diabetes, islet cells in the pancreas can’t produce enough insulin and other hormones that control blood glucose (sugar). If left uncontrolled, this leads to dangerously high levels of glucose in the blood that may result in tissue and organ damage and early death.

So, finding genes that promote insulin secretion could be a valuable source of treatment strategies for type 2 diabetes. And that’s just what researchers in the lab of biochemistry professor Alan Attie at the University of Wisconsin–Madison and collaborators at The Jackson Laboratory discovered when comparing the genetic variations associated with type 2 diabetes in humans with those of a special, genetically diverse mouse population fed on a diet high in fat and sugar.

The work, published in the journal Genetics, is the first to show how a Western-style diet alters the regulation of genes in the pancreatic islets of mice. It also demonstrates that the Diversity Outbred (DO) mouse population can stand in for humanity in laboratory studies of genetic risk variants found in human genome-wide association mapping.

This press release was written by Joyce Dall'Acqua Peterson of The Jackson Laboratory and was originally published on their news site.